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Background: Both human and mouse allergic contact dermatitis (ACD) frequently demonstrates a combined type 1 and type 2 immune response. However, the relative importance of type 2 immunity in this setting has been incompletely understood yet.
Objective: To explore an effector function of type 2 immunity in ACD with mixed type 1/type 2 immune response.
Methods: Gene expression characteristics of contact hypersensitivity (CHS) model was examined by quantitative polymerase chain reaction. Cytokine profile of T cells was analyzed by flow cytometry. The involvement of type 2 immunity was assessed by antibody-mediated cytokine neutralization and cell depletion. The role of specific subset of cutaneous dendritic cells was evaluated using diphtheria toxin-induced cell-depleting mouse strains.
Results: Oxazolone-induced CHS revealed a combination of type 1/type 2 gene expression. The severity of oxazolone-induced CHS was ameliorated by neutralization of IL-4 but not of IFN-γ, indicating that type 2 immunity plays a dominant effector function in this mixed type 1/type 2 model. Mechanistically, type 2 effector immunity was mounted by CD301b+Langeirn- dermal dendritic cells in part through thymic stromal lymphopoietin-interleukin 7 receptor alpha signaling-dependent manner.
Conclusion: Our findings suggest the clinical rationale for targeting type 2 immunity as a relevant therapeutic strategy for the mixed immune phenotype of ACD.
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http://dx.doi.org/10.1016/j.jdermsci.2021.10.001 | DOI Listing |
Future Oncol
September 2025
Department of General Surgery, Institute of General Surgery, Northern Jiangsu People's Hospital Affiliated to Yangzhou University, Yangzhou University, Yangzhou, China.
Immune checkpoint therapy has demonstrated significant potential in the treatment of various solid tumors. Among these, tumor-induced immunosuppression mediated by programmed cell death protein 1 (PD-1) represents a critical checkpoint. PD-1/programmed death-ligand 1 (PD-L1) inhibitors have been proven to exhibit substantial efficacy in solid tumors such as melanoma and bladder cancer.
View Article and Find Full Text PDFRev Med Liege
September 2025
Service de Diabétologie, Nutrition et Maladies métaboliques, CHU Liège, Belgique.
Type 1 diabetes (T1D) is an autoimmune chronic disease that leads to the destruction of pancreatic beta cells and thus requires lifelong insulin therapy. Constraints and adverse events associated to insulin therapy are well known as well as the risk of long-term complications linked to chronic hyperglycaemia. Symptomatic T1D is preceded by a preclinical asymptomatic period, which is characterized by the presence of at least two auto-antibodies against beta cell without disturbances of blood glucose control (stage 1) or, in addition to immunological biomarkers, by the presence of mild dysglycaemia reflecting a defect of early insulin secretion (stage 2).
View Article and Find Full Text PDFJ Innate Immun
August 2025
Piezo-type mechanosensitive ion channel component 1 (Piezo1) is an evolutionarily conserved and multifunctional mechanosensitive ion channel protein that has emerged as a significant contributor to the pathogenesis of inflammatory bowel disease (IBD). Piezo1 plays a crucial role in regulating intestinal barrier integrity, immune responses, and the intestinal nervous system, thereby influencing disease progression. Its expression patterns correlate with disease severity and inflammatory markers in IBD patients, indicating its potential as a diagnostic and prognostic biomarker.
View Article and Find Full Text PDFEMBO J
September 2025
Department of Bacterial Infection and Host Response, Graduate School of Medical and Dental Sciences, Institute of SCIENCE TOKYO, 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan.
Many enteric bacterial pathogens deliver virulence effectors to counteract host innate immune responses, such as inflammation and cell death, and colonize the intestinal epithelium. However, host cells recognize the disruption of their innate immune signaling by bacterial effectors and induce alternative immune responses, collectively termed "effector-triggered immunity", to clear bacterial pathogens. Here, we describe a mechanism of cell death induction via effector-triggered immunity and the bacterial countermeasures of the pathogen Shigella flexneri.
View Article and Find Full Text PDFNature
September 2025
Department of Laboratory Medicine and Pathology, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Alberta, Canada.
Cancer-associated muscle wasting is associated with poor clinical outcomes, but its underlying biology is largely uncharted in humans. Unbiased analysis of the RNAome (coding and non-coding RNAs) with unsupervised clustering using integrative non-negative matrix factorization provides a means of identifying distinct molecular subtypes and was applied here to muscle of patients with colorectal or pancreatic cancer. Rectus abdominis biopsies from 84 patients were profiled using high-throughput next-generation sequencing.
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